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Somatosensory timing and cerebellar-basal ganglia beta-band interactions in Parkinson's disease

Pando-Naude, V.; Andersen, L.

2025-05-15 neuroscience
10.1101/2025.05.15.653735 bioRxiv
Show abstract

Rhythmic cognition relies on the interplay between endogenous and exogenous temporal structures, allowing organisms to anticipate and adapt to events in time. Neural oscillations, particularly in the beta band (14-30 Hz), are central to this predictive capacity, coordinating sensorimotor networks that support timing and rhythm perception. Parkinsons disease, a movement disorder characterized by disrupted basal ganglia function, offers a unique framework to probe the neural mechanisms underlying rhythmic cognition. We measured beta-band activity and connectivity across cerebellum, basal ganglia, thalamus and motor cortex during a rhythmic somatosensory timing task to compare prediction- and evaluation-related activity between participants with Parkinsons disease and controls. Using magnetoencephalography, participants received tactile stimuli in regular (non-jittered) and irregular (jittered) sequences, with the final stimulus omitted to probe prediction before and evaluation after the omission. We found prediction-related differences between participants with Parkinsons disease and controls in cerebellum and basal ganglia before the omissions, while replicating earlier findings in controls, showcasing cerebellar evaluation responses after the omissions. In Parkinsons disease, basal ganglia activity favored jittered over non-jittered somatosensory rhythms, opposite to controls. Altered cerebellar beta-band responses correlated with Parkinsons disease symptom severity. Connectivity analyses revealed group-by-regularity interactions in a sensory-integration network. These findings demonstrate that temporal prediction and evaluation in rhythmic cognition rely on coordinated beta-band dynamics across the cerebello-striatal-thalamo-cortical network. In Parkinsons disease, disrupted basal ganglia function shifts the network toward compensatory cerebellar engagement and increased connectivity demands under irregular temporal conditions, exposing core mechanisms by which the brain encodes and adapts to rhythmic structure.

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